While all tissues age into dysfunction, the primary cause of human mortality is the aging of the cardiovascular system into heart failure, stroke, and heart attack, combined with the consequences of progressively worsening cardiovascular function in other organs. The way in which cardiovascular aging manifests is well documented, and the underlying processes of aging that contribute to the observed outcomes are also fairly well understood at the high level. The challenge lies in establishing exactly how the low-level mechanisms of aging give rise to changes and loss of function in the heart and vasculature. This is a task that may not even be needed, if instead the research community focused on ways to repair the molecular damage of aging. We don’t need to fully understand how exactly any specific harm contributes to cardiovascular disease if we build a means to address it and observe benefits to result from the use of that therapy.
Aging is a slow, progressive, and inevitable process that affects multiple organs and tissues, including the cardiovascular system. The most frequent cardiac and vascular alterations that are observed in older adults (especially patients aged ≥80 years) are diastolic and systolic dysfunction, progressive stiffening of the vascular wall and endothelial impairment usually driven by an excess of extracellular matrix (ECM) and profibrotic substances, reduced levels of matrix metalloproteinases (MMPs), or by amyloid and calcium deposits in myocardium and valves (especially in aortic valves). Moreover, deformation of the heart structure and shape, or increased adipose tissue and muscle atrophy, or altered ion homeostasis, chronotropic disability, reduced heart rate, and impaired atrial sinus node (SN) activity are other common findings.
Interestingly, aging is often associated with oxidative stress, alterations in the mitochondrial structure and function, and a low-grade proinflammatory state, characterized by high concentrations of cytokines and inflammatory cells, without evidence of infectious pathogens, in a condition known as ‘inflammaging‘. Aging is a well-recognized independent risk factor for cardiovascular disease and easily leads to high mortality, morbidity, and reduced quality of life. Recently, several efforts have been made to mitigate and delay these alterations, aiming to maintain overall health and longevity. The primary purpose of this review was to provide an accurate description of the underlying mechanisms while also exploring new therapeutic proposals for oxidative stress and inflammaging. Moreover, combining serum biomarkers with appropriate imaging tests can be an effective strategy to stratify and direct the most suitable treatment.
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